Designs For Health Research & Education Blog

Spring has sprung, the flowers are out, and if you’re not planning and planting your garden, stake out your local farmers’ markets. Of the myriad reasons to do so, chances are extremely high that you need some potassium. 93% of us do, according to the National Health and Nutrition Examination Survey (NHANES). No better way to get it than lots of fresh fruits and veggies. (Or avocado and coconut water -- my two favorite sources.)

For you skimmers, I’ll skip to the punchline of this ENL: If we had to pick one single, easy fix for the impending 47,000,000,000,000 US dollar global health care crisis it would be INCREASE FOOD SOURCE POTASSIUM. That’s it. We’d shave 20-30% right off the top of that debt. Done. And there would be a trickle-down effect of a healthy diet beyond that immediate savings, too. 

Schizophrenia is a devastating mental illness that usually strikes in late adolescence or early adulthood, but can crop up at any time in life. The signs and symptoms vary from individual to individual, but all people with the disorder show one or more symptoms, including auditory hallucinations, paranoid or bizarre delusions, or disorganized speech and thinking. It is also accompanied by significant social or occupational dysfunction.

While schizophrenia appears to be a rare condition, the numbers say something different. Each year, 100,000 people will be diagnosed with the illness in the United States alone while in total, over 2 million in the U.S. suffer with schizophrenia. That’s more than the number of people who are ill with multiple sclerosis, muscular dystrophy and insulin-dependent diabetes combined.

It is important to note that contrary to popular belief and perhaps certain stereotypes propagated by the film industry, a person with schizophrenia does not have a split personality. Schizophrenia is a psychosis in which a person cannot tell what is real from what is imagined.

Organically, abnormalities in the hippocampus region of the brain are among the most consistent findings in schizophrenia research. Interestingly, these same abnormalities are implicated in bipolar disorder.

Coconut oil may be one of the most misunderstood of the more readily available dietary fats/oils. As it is predominantly over 90% saturated fat, consumers assume it is bad for you and look for other seemingly less offensive alternatives.

The distinguishing feature between coconut oil and other forms of saturated fats and triglycerides is the much shorter length of the fatty acid. Coconut oil is actually a medium chain triglyceride (MCT), 6 to 12 carbon lengths long, as opposed to long chain triglycerides which are over 12 carbon lengths long and is the principal form of fat found in western diets. This smaller chain length makes it much easier for the body to absorb, digest and process as its breakdown requires less energy and less enzymatic action than what is usually needed for the longer chain triglycerides. Once broken down into medium chain fatty acids and absorbed in the body, they are then delivered to the liver where they are used as a primary source of energy. This leads to an increase in metabolism, ultimately resulting in an improvement in blood lipid profiles. Indeed, in eastern Asian cultures where coconut oil is a significant source of fat, rates of atherosclerosis and coronary heart disease are lower than their western counterparts.

Wide array of clinical uses

Clinically and therapeutically, coconut oil appears to possess a variety of useful properties that may make it, when used appropriately, a no-brainer as a food item to be consumed on a daily basis for many people.

As part of a weight loss protocol, coconut oil has been shown to help improve anthropomorphic profiles in overweight and obese men and women.

Gastrointestinal biofilms are an important topic, and those comprised of pathogenic microbes are getting much well-deserved attention in the integrative medical community. However, in keeping with the sIgA topic, I want to give a shout-out to commensal biofilms, which are vital to GI health and deserve similar attention. 

Biofilms are everywhere, allowing bacteria to survive -- good or bad. They are found at the solid-liquid interface in most environments. Indeed, dental plaque is a biofilm, as is the slime on an icky bathtub. Biofilms are comprised of bacteria (and/or other microbes) and an extracellular matrix of excreted polymeric polysaccharides. 

Simply put: bugs + goo = slime (biofilm). 

Slime is nothing to joke about! Biofilms allow pathogenic organisms to be antibiotic resistant, up to 1000-fold by one estimate. But biofilms comprised of commensals can be our friends, modulating our immune response, supporting GI integrity and reducing inflammation. 

Research on commensal GI biofilm shows that E. coli , bifidobacteria and L. reuteri are apparently efficient producers, with the former mediated by sIgA and mucin. Research suggests commensal biofilms may be anti-inflammatory, modulate cytokine production and crowd out pathogenic biofilms.

One study in rats with human-type flora showed improved bifidobacteria biofilm, mucus thickness, villous height, crypt depth, and mucin-producing goblet cell numbers when supplemented with inulin-type fructans. How cool is that? 

How can we tell if our GI commensal biofilm is healthy? 

On a stool test, I would be concerned if I didn’t see enough bifidobacteria, lactobacillus, commensal E. coli or sIgA. Glutamine, vitamin A and S. boulardii support sIgA production; whereas the inulin mentioned above, plus probiotic supplementation, will help facilitate commensal bacterial growth. Finally, treating inflammation and minimizing unwarranted antibiotic use should also benefit biofilm status. 

Evidence is making it very clear that there is a strong association between gut health, brain function and mood. While it has long been known that stress can wreak havoc with our digestive tract, problems in the GI tract can also negatively impact the brain, causing anxiety and depression. In other words, what is transpiring in your gut may directly influence central nervous system function, influencing neural circuitry, and can therefore have an effect (positive or negative) on behavior.

The newest research suggests, for instance, that how your digestive tract evolves in the first few years of life can influence the health of your brain and subsequently your behavior in the future. This hypothesis is predicated upon the way in which a healthy GI floral population positively influences neurons involved in motor control and behavior.  In the case of those with overwhelming populations of gut pathogens or gut dysbiosis, it can pave the way for the development of anxiety and depression later in life.

As gut health and gastrointestinal compromise can be a mechanism for the origins of systemic inflammation and autoimmunity, and since both inflammation and autoimmune conditions have also been associated with the genesis of mood disorders, it is only reasonable to suggest, again, that an intimate relationship between gut health, brain function and mental health exists. As one recent study demonstrates, inflammatory bowel disease in animal experiments can have an adverse effect on the hypothalamus by increasing the sensitivity of the HPA axis to stress.

Regarding the inflammatory process and depression, one study went so far as

A recent study published in the journal Nature Medicine associates the amino acid L-carnitine, found in red meat, supplements, and sports supplements, with the risk of heart disease. Here are some examples of what the media said about it: The Daily Mail (UK): “Red meat nutrient used in weight-loss and muscle-building supplements could cause heart disease”! The Dallas News: “Put down that steak! (and energy drinks, too); the carnitine in these foods may increase risk of cardiovascular disease”!

Here is the gist of the study:

• a diet high in L-carnitine promotes the growth of certain bacteria that metabolize the amino acid;
• during that metabolization, an organic compound called trimethylamine-N-oxide (TMAO) is produced in the blood; and
• this compound increases risk of heart disease.

The study further states that vegetarians and vegans have different gut bacteria, which do not produce a burst of TMAO after consuming L-carnitine.

There is a lot to find fault with in this study.

First, there’s the question of the study participants. Most of the study was done on mice, though there was a human component—a tiny sample of only six people, five meat-eaters and one vegan. That’s right, their conclusion that vegetarians and vegans have different gut bacteria that don’t produce a burst of TMAO after consuming L-carnitine was based on just one individual.

Arteriosclerosis refers to stiffening or hardening of the arteries where atherosclerosis, on the other hand, is a specific type of arteriosclerosis (although the terms are sometimes used interchangeably). Atherosclerosis refers to the buildup of fats and cholesterol in and on your artery walls (plaques), which can restrict blood flow. Then there is peripheral arterial disease (P.A.D.). Similarly, P.A.D. is a disease in which plaque builds up in the arteries but it also can affect the arteries that carry blood from your heart to your head, arms, kidneys, and stomach.

Inflammation

The etiology that sets in motion the processes that initiate the creation of arteriosclerosis may vary but there are particular pathways involved in its progression that have been solidly indentified. Inflammation is one of these processes.

Inflammation is defined as a response to injury from infectious, physical, or chemical agents. It is now widely accepted that inflammation plays a major role in the development and progression of atherosclerosis, where the initial injury is damage to the endothelial cells lining the blood vessels. Some of the factors leading to this injury include increased levels of oxidized low density lipoproteins (for instance, free radicals formed by cigarette smoking), possible infectious agents, and the shearing stress placed on endothelial cells due to hypertension.

Injury to the endothelial cell wall triggers a cascade of events and the secretion of mediators that modulates the inflammatory response. This includes the release of a variety of cytokines including TNF-α, NFκβ and chemokines such as monocyte chemoattractant protein-1 (MCP-1) and the vascular cell adhesion molecule-1 (VCAM-1). This causes an influx of leukocytes, monocytes and platelets to adhere to the cell wall, where the monocytes are then able to migrate across the endothelial barrier into the intima layer and differentiate into macrophages. The macrophages then phagocytize the increased amount of lipoproteins from the LDLs and transform into foam cells. The newly formed foam cells secrete pro-inflammatory molecules such as interleukin-1 (IL-1), interleukin-6 (IL-6), and TNF-α; all of which can contribute to additional leukocyte accumulation and induce smooth muscle proliferation and migration from the medial layer into the intima. The arterial wall begins to thicken as more LDLs are taken up by macrophages and an atheroma is formed.

My 53-year-old male patient is in the waiting room.  Sweating a little. Blood pressure 143/90 – moderately elevated (it’s usually 125/80). This great guy, a patient of mine, father of 3, is anxiously waiting to have his PSA blood drawn.

What is PSA? 

Among physician’s it’s jokingly short for “Patient Stimulated Anxiety. “ It really stands for Prostate Specific Antigen – a misnomer. It turns out that PSA is found in many other tissues and fluids other than the prostate. In males, there are PSA molecules in semen, for example.

In women, PSA molecules are found in female ejaculate (that’s right, females ejaculate too – I know you did not know that), in breast milk and amniotic fluid.

Here’s the kicker; PSA is found in a women’s blood who have cervical, uterine and breast cancer (Pummer et al. 1992, Mohajeri et al. 2011).

Ok, sorry to digress a little. I have not answered the questions  – what is PSA?

PSA is a sugar molecule combined with a protein (referred to a glycoprotein in the scientific community). Its main role is to liquefy semen. You may have noticed that semen clumps up initially after ejaculation. Within a few minutes it liquefies due to the function of the molecule PSA. This “anti-clumping” aspect is important for procreation. Sperm cells swim better when they are loose and free.

PSA and men before Prostate Cancer diagnosis

Anything under 4ml/ng does not mean you don’t have prostate cancer.  In fact, 15% of men with a PSA under 4 develop prostate cancer (Thompson et al. 2004)

Generally speaking PSA is age related. For example, a 40-year-old should have a PSA well under 1.0ml/ng (exception to the rule, this individual may have an infection of his prostate causing his PSA to be above 4).

A 60 year-old with a PSA of 2 may be fine.

A steady trend upward, even if the number is under 4,  after three or four PSA tests may be more connected to prostate cancer once prostatitis or other benign conditions are ruled out.

FYI – prostate enlargement or BPH may also cause the PSA to increase.

Other causes of false alarms:

1. The finger before the blood draw.  That’s right, a digital prostate exam before the blood draw will cause the PSA number to be higher (Collins et al. 1997).

You’d be surprised how many physicians’ do this >:-(.

Take charge. If you’re going to get the finger, get it after the blood draw.

The Standard American Diet or S.A.D. is well-known to nutritionists and most healthcare providers as being associated with high amounts of processed foods and refined carbohydrates. Unfortunately, these foods are completely devoid of their inherent nutrition and fiber while also often being high in sugar and unhealthy fats. Throw in copious amounts of salt, high fructose corn syrup, artificial ingredients (such as flavors, preservatives and colorants) and a lack of consistent exercise and you have a recipe for epidemic rates of cardiovascular disease, diabetes and a variety of cancers.

These physiological responses to what has become a diet of convenience (it actually requires some work, time and effort to cook healthy, unprocessed foods) also translate to other cultures. As many second and third world countries become more prosperous, their demands for all things western also increase. This includes access and desire for western types of food. We have seen the effects of adopting western ways of eating on traditional cultures as diverse as Chinese and African peoples, as they end up experiencing dramatically increased rates of diabetes, obesity and cancer once they transition from a traditional, predominantly whole plant food diet to one composed of processed foods.

Rheumatoid arthritis, or RA, is not only a form of inflammatory arthritis but also an autoimmune disease that primarily attacks the body’s own tissues, specifically the synovium, a thin membrane that lines the joints. As a result of the attack, fluid builds up in the joints, causing pain and inflammation that can occur throughout the entire body. And because the disease can also cause inflammation and injury in other organs in the body, rheumatoid arthritis is referred to as a systemic illness and is sometimes called rheumatoid disease.

Rheumatoid arthritis is characterized by periods of disease flares and remissions, and can cause permanent joint destruction and deformity. In addition to causing joint problems, rheumatoid arthritis can also affect your whole body with fevers and fatigue.

The etiology of the disease is complex and probably multifactorial. Current research supports the notion that RA is caused by a combination of genetic and environmental factors, as specific genetic markers have been identified with the condition. While not all individuals who have the genetic predisposition for the disease actually gets the disease, it is reasonable to believe that environmental factors will act on an epigenetic level, activating these associated genes. There is also evidence that chronic viral infections may play a role in the disease’s pathogenesis.

Additionally, it also appears that gut microflora balance may have a crucial role in the instigation of the condition. Disturbances in the microflora environment causing disruptions in the delicate microflora balance has been shown to increase populations of pathological bacteria. These bacteria go on to produce inflammatory cytokines such as interleukin 17 and proinflammatory Th17 cells, both of which have been associated with the pathophysiology of rheumatoid arthritis and autoimmunity in general.